Skeletal muscle plays a central role in metabolic adaptations to increasing and decreasing physical activity, in disease (e.g. cachexia), in obesity, and in aging (e.g. sarcopenia). Sarcopenia is described as the age-associated loss of skeletal muscle (Evans (1995) J. Gerontol. 50A:5-8) and has been associated with mobility disability (Janssen and Ross, (2005) J. Nutr. Health Aging 9:408-19) and greatly increased health-care costs for elderly people (Janssen et al. (2004) J. Am. Geriatr. Soc. 52:80-5). Loss of skeletal muscle with advancing age is associated with decreased energy requirements and concomitant increase in body fatness, weakness and disability, insulin resistance and risk of diabetes. Loss of skeletal muscle associated with an underlying illness (cachexia) is associated with a greatly increased mortality (Evans (2008) Clin. Nutr. 27:793-9).
Because of the important role total body skeletal muscle mass plays in aging and disease, there is an effort in the pharmaceutical arts to identify therapeutic agents that will stimulate muscle protein synthesis and increase muscle mass. However, current methodologies for quantification of muscle synthesis and muscle mass often involve invasive procedures (e.g. muscle biopsies) or rely on expensive equipment (i.e. DEXA, MRI, or CT) that provides only indirect data on whole body muscle mass. Because of these limitations, no method is routinely used in the clinic for estimation of skeletal muscle mass, and no diagnostic criteria for estimates of muscle mass have been produced. As a result, there is a no straightforward way to determine the effects of potential therapeutic agents on muscle protein synthesis mass.
Accordingly, there remains a need in the art for reliable, easily-performed, non-invasive measurements of total body skeletal muscle mass.